In the age of antibiotics, vaccines, and other medical innovations, life expectancy has increased worldwide, leading to an increased prevalence of chronic diseases. In the US alone, the Department of Health and Human Services estimates that by 2040 82.3 million Americans (21.7% of the population) will be over 65 years old. As a result, age-related diseases, which cause significant morbidity and mortality, will become a rising public health problem.
There is also an increase in the prevalence of multimorbidity defined by the coexistence of two or more chronic pathologies in the same individual. Studies show that the range of multimorbidity in individuals over 60 years old is between 55% and 98%. Multimorbidity is associated with functional decline, disability, lower quality of life, higher rates of emergency care and hospitalization, polypharmacy, and increased healthcare costs, all of which are a major burden on the community.
The concept of cognitive impairment has been carefully analyzed over the past two decades, given the devastating consequences of this problem, especially among older populations. Cognitive function can be divided into six major areas: language (verbal fluency and comprehension), learning ability and memory (working memory and memory-based labeling), attention, executive functions (planning and problem solving), praxis (motor-intellectual, cognitive, and visual constructive). and visual-spatial functions.
Mild cognitive impairment (MCI) is defined as a cognitive dysfunction that is more severe than normal age-related cognitive decline or education level, but not so severe that it significantly affects daily function. MCI exceeds the “age-related” decline in cognition experienced by healthy individuals, but does not meet the criteria for dementia. Moreover, not all cases of MCI progress towards dementia.
In the general population, studies have shown that the prevalence of MCI in older adults is between 10 and 20%. However, cognitive impairment is largely underdiagnosed and under-treated by primary care physicians. There are several screening tools that can identify those at high MCI risk, such as Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Saint Louis University Mental Status Examination (SLUMS), or Rapid Cognitive Screen. Once the diagnosis of cognitive dysfunction has been determined, it is important to determine the etiology and contributing factors and evaluate if there are any reversible causes. Every practitioner should be familiar with these questionnaires, especially MMSE, and use them when an MCI is suspected.
Neuroanatomical structures and functions can be evaluated with neuroimaging techniques. Computed tomography (CT) scanning and magnetic resonance imaging (MRI) can analyze brain structure and exclude conditions such as stroke, brain tumors, or vascular malformation. Fluorodeoxyglucose positron emission tomography (FDG-PET) scan, which is mostly used for research purposes, can evaluate brain function and appears to be more sensitive than MRI in the diagnosis of MCI. This tool uses a radioactive glucose tracer that binds to highly active brain regions. The presence of hypometabolic areas in the temporal or parietal lobe is a sign of neurodegeneration. Subjects who develop these hypometabolic areas have a higher risk of progressing from MCI to dementia. For research purposes, there are several biomarkers used for the diagnosis of MCI and dementia, but the lack of standardization of optimal breakpoints limits their clinical use.
There are well-established risk factors for MCI development: age, male gender, family history of cognitive impairment, presence of the apolipoprotein E allele, smoking, and low education level. Moreover, in a study aimed at determining whether multimorbidity is a risk factor for mild cognitive impairment and dementia, individuals who associate at least two of the following, hypertension, hyperlipidemia, coronary artery disease and arthritis, were found to be at very high risk. Recent studies have shown that certain chronic respiratory conditions, such as chronic obstructive pulmonary disease (COPD), obstructive sleep apnea (OSA), or idiopathic pulmonary fibrosis (IPF), have a significant impact on cognitive function. There are differences in the prevalence of reported cognitive dysfunction among the conditions listed above, and these can be explained by study design and limitations. These are as follows;
Diagnostic methods (psychometric tools or neuroimaging) for cognitive impairment,
Small sample size or inappropriate control group,
• Moment of evaluation (steady phase / flammability)
The severity of airflow limitation, the presence of hypoxia, and the use of long-term oxygen therapy
Multiple mixers can also contribute to a wide variety of data on prevalence: age, education level, smoking history, comorbidities, etc.
Cognitive Impairment in Obstructive Sleep Apnea
Sleep apnea syndrome is a breathing disorder during sleep characterized by total or partial obstruction of the upper airways and increased breathing effort, leading to hypoxia and hypercapnia. These properties produce micro-awakenings that cause sleep disturbance and changes in neuronal activity. These are all potential mechanisms for cognitive impairment.
In adults, the prevalence of OSA increases significantly with age. Between the ages of 30 and 49, with an increasing prevalence over 50-70 years and among postmenopausal women, 10% of men and 3% of women are diagnosed, increasing to 17% and 9% respectively. Due to the increase in obesity among the population of developing countries, these percentages are higher than those published 10 years ago. Even more worryingly, the actual prevalence can be underestimated as many people with OSA are not diagnosed.
Nighttime symptoms are loud snoring, unrestful sleep, nocturia, sweating and dry mouth. One of the most common daytime symptoms in OSA patients is daytime sleepiness. This greatly affects the quality of life and cognitive performance. OSA has been associated with a wide variety of psychological problems, including depression, anxiety, neurocognitive dysfunction, particularly attention, wakefulness, memory and learning, phenomena associated with sleep disruption, and intermittent hypoxemia. The relationship between sleep disruption, sleep deprivation and excessive daytime sleepiness are suggested mechanisms underlying cognitive impairment through its effects on attention. The exact prevalence of cognitive disorders and the severity of this syndrome due to multiple comorbidities are unknown in adult patients with OSA.
Risk Factors for Cognitive Deficits in OSA Patients
There are numerous comorbidities of OSA that can affect cognitive function, such as treatment-resistant hypertension, diabetes, COPD, congestive heart failure, stroke, smoking, and alcoholism. In addition, age, gender (male), obesity, and the use of psychoactive drugs are considered independent risk factors. Aging itself causes a decrease in cognitive function and the presence of OSA in these patients causes more brain damage, although cognitive impairment is more obvious. It is also known that smoking increases the risk of both vascular and Alzheimer’s dementia and neurocognitive decline not associated with dementia through its detrimental effects on blood vessels and circulation.
Another important factor between OSA and cognitive decline, it seems, is the genetic factor. Therefore, studies show that the presence of apolipoprotein E4 (ApoE4) is associated with an increased incidence of cognitive impairment. High blood pressure is associated with cognitive decline, both when isolated and in the presence of metabolic syndrome, particularly due to the presence of cardiovascular risk factors. In addition, the presence of hypothyroidism in OSA patients can accelerate cognitive decline, and the available data are not sufficient to show whether treatment improves the decline phenomenon.
Moderate alcohol consumption may protect against dementia, but it is associated with cognitive impairment manifested by significant alcohol consumption, memory loss, impaired personality, and impaired judgment. Alcohol intake before going to bed affects sleep structure and also, depending on the amount, instability of the upper airways may increase. Therefore, excessive alcohol use in OSA patients may cause more severe cognitive deficits. Another common comorbidity of OSA is stroke independently accompanied by a cognitive deficit and even dementia. Studies show that up to 30% of stroke patients can develop dementia. And psychoactive medications like benzodiazepines, narcotics, and barbiturates can exacerbate OSA and increase attention and alertness issues.
Studies conducted over time have shown that there are structural and functional changes in the brain and this causes cognitive deficiency. There are studies showing a decrease in gray matter in the hippocampus with MRI techniques; cerebellum; frontal, parietal and temporal lobes; as well as the anterior cingulate cortex. Also, a reduction in the hippocampus, which plays an important role in memory consolidation, has been observed. White matter changes reported by researchers; shows that axonal or glial pathology is also present in OSA, in line with other previous findings.
Author: Ozlem Guvenc Agaoglu